Inflammatory response self-limitation

Diarrhea is a common problem that is usually self-limiting and of short duration. Increased accumulations of small intestinal and colonic contents are known to be responsible for producing diarrhea. The former may be caused by increased intestinal secretion which may be enterotoxin-induced, eg, cholera and E. col] or hormone and dmg-induced, eg, caffeine, prostaglandins, and laxatives decreased intestinal absorption because of decreased mucosal surface area, mucosal disease, eg, tropical spme, or osmotic deficiency, eg, disaccharidase or lactase deficiency and rapid transit of contents. An increased accumulation of colonic content may be linked to increased colonic secretion owing to hydroxy fatty acid or bile acids, and exudation, eg, inflammatory bowel disease or amebiasis decreased colonic absorption caused by decreased surface area, mucosal disease, and osmotic factors and rapid transit, eg, irritable bowel syndrome. 

Hapten-specific CD8+ T lymphocytes, likely the major effector population, are directly cytotoxic to chemical exposed keratinocytes and also release cytokines that boost the inflammatory response. In addition, Thl cells release a number of cytokines and chemokines that promote inflammation and activate mast cells and, in the presence of IFNy, are also capable of killing keratinocytes. Although the hapten may persist in skin for some time, this reaction is self-limited. CD4+ regulatory T cells that secrete IL-10 (similar to those described in relation to UV-induced immune suppression in Section 32.4.3) appear to play an important role in this regulation. 

The causal relationship between inflammation, innate immunity, and cancer is now widely accepted. Normal inflammation is self-limiting because the production of proinflammatory cytokines is followed by that of anti-inflammatory cytokines. In tumors, the inflammatory process persists. Chronic inflammation seems to be due to persistence of the initiating factors or failure of mechanisms that are required to resolve the inflammatory response [139]. The strongest association of chronic inflammation with malignant diseases is in colon carcinogenesis in patients with inflammatory bowel diseases such as chronic ulcerative colitis and Crohn s disease. 

Chua et al. (C6) reported markedly, but transiently, elevated levels of proMMP-9 and TIMP-1 in the plasma of patients with Kawasaki disease (an acute, self-limiting vasculitis) this data is consistent with MMP-9 involvement in vascular remodeling and an inflammatory response to a microbial agent. Matsuyama et al. (M9) reported that circulating levels of MMPs can be useful in the diagnosis of Takayasu arteritis. 

After women have tried lifestyle changes, nutritional supplements, and nonpharmacologic treatment approaches, some may require pharmacologic therapies if there is limited response. Women with less severe PMS generally self-treat headaches and cramps with aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs (NSAlDs). NSAIDs, such as naproxen and ibuprofen, are the treatments of choice for dysmenorrhea, menstrual headaches or migraines, and mastalgia. 

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